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Advances in Immunology and Inflammation During and After Infectious Diseases
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Advances in Immunology and Inflammation During and After Infectious Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 7385

Special Issue Editor

Dr. Manuela Ceccarelli

E-Mail Website
Guest Editor
Unit of Infectious Diseases, Department of Medicine and Surgery, “Kore” University of Enna, Enna, Italy
Interests: HIV; metabolomics; antimicrobial stewardship; cardiovascular disorders in HIV
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, our knowledge regarding the role of inflammation and immune response during and after infectious diseases has improved. For instance, let us refer to sepsis definition and pathogenesis, or to the COVID-19 emergency. But inflammation and immune response during and after infectious diseases can also lead to serious consequences, such as cancers, metabolic disorders, and cardiovascular diseases.

With this Special Issue, we aim to provide new insights into immune response and inflammation, and especially persistent inflammation, in infectious diseases. Moreover, we aim to shed light on the immune response mechanisms which might help in developing new treatment strategies.

Original and review articles, including basic studies, are all welcome to be submitted to this Special Issue. Research topics may include, but are not limited to, the following:

  • Molecular and cellular mechanisms governing the immune response to microorganisms;
  • Molecular and cellular mechanisms involved in persisting symptoms after the resolution of infection (i.e., long COVID-19);
  • Therapeutic application of molecular and cellular patterns.

Dr. Manuela Ceccarelli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bacterial infections
  • fungi infections
  • HIV
  • COVID-19
  • immune response
  • inflammation

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Published Papers (5 papers)

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Research

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20 pages, 2161 KiB  
Article
Persistent Monocytic Bioenergetic Impairment and Mitochondrial DNA Damage in PASC Patients with Cardiovascular Complications
by Dilvin Semo, Zornitsa Shomanova, Jürgen Sindermann, Michael Mohr, Georg Evers, Lukas J. Motloch, Holger Reinecke, Rinesh Godfrey and Rudin Pistulli
Int. J. Mol. Sci. 2025, 26(10), 4562; https://doi.org/10.3390/ijms26104562 - 9 May 2025
Viewed by 1980
Abstract
Cardiovascular complications are a hallmark of Post-Acute Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection (PASC), yet the mechanisms driving persistent cardiac dysfunction remain poorly understood. Emerging evidence implicates mitochondrial dysfunction in immune cells as a key contributor. This study investigated [...] Read more.
Cardiovascular complications are a hallmark of Post-Acute Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection (PASC), yet the mechanisms driving persistent cardiac dysfunction remain poorly understood. Emerging evidence implicates mitochondrial dysfunction in immune cells as a key contributor. This study investigated whether CD14++ monocytes from long COVID patients exhibit bioenergetic impairment, mitochondrial DNA (mtDNA) damage, and defective oxidative stress adaptation, which may underlie cardiovascular symptoms in PASC. CD14++ monocytes were isolated from 14 long COVID patients with cardiovascular symptoms (e.g., dyspnea, angina) and 10 age-matched controls with similar cardiovascular risk profiles. Mitochondrial function was assessed using a Seahorse Agilent Analyzer under basal conditions and after oxidative stress induction with buthionine sulfoximine (BSO). Mitochondrial membrane potential was measured via Tetramethylrhodamine Ethyl Ester (TMRE) assay, mtDNA integrity via qPCR, and reactive oxygen species (ROS) dynamics via Fluorescence-Activated Cell Sorting (FACS). Parallel experiments exposed healthy monocytes to SARS-CoV-2 spike protein to evaluate direct viral effects. CD14++ monocytes from long COVID patients with cardiovascular symptoms (n = 14) exhibited profound mitochondrial dysfunction compared to age-matched controls (n = 10). Under oxidative stress induced by buthionine sulfoximine (BSO), long COVID monocytes failed to upregulate basal respiration (9.5 vs. 30.4 pmol/min in controls, p = 0.0043), showed a 65% reduction in maximal respiration (p = 0.4035, ns) and demonstrated a 70% loss of spare respiratory capacity (p = 0.4143, ns) with significantly impaired adaptation to BSO challenge (long COVID + BSO: 9.9 vs. control + BSO: 54 pmol/min, p = 0.0091). Proton leak, a protective mechanism against ROS overproduction, was blunted in long COVID monocytes (3-fold vs. 13-fold elevation in controls, p = 0.0294). Paradoxically, long COVID monocytes showed reduced ROS accumulation after BSO treatment (6% decrease vs. 1.2-fold increase in controls, p = 0.0015) and elevated mitochondrial membrane potential (157 vs. 113.7 TMRE fluorescence, p = 0.0179), which remained stable under oxidative stress. mtDNA analysis revealed severe depletion (80% reduction, p < 0.001) and region-specific damage, with 75% and 70% reductions in amplification efficiency for regions C and D (p < 0.05), respectively. In contrast, exposure of healthy monocytes to SARS-CoV-2 spike protein did not recapitulate these defects, with preserved basal respiration, ATP production, and spare respiratory capacity, though coupling efficiency under oxidative stress was reduced (p < 0.05). These findings suggest that mitochondrial dysfunction in long COVID syndrome arises from maladaptive host responses rather than direct viral toxicity, characterized by bioenergetic failure, impaired stress adaptation, and mitochondrial genomic instability. This study identifies persistent mitochondrial dysfunction in long COVID monocytes as a critical driver of cardiovascular complications in PASC. Key defects—bioenergetic failure, impaired stress adaptation and mtDNA damage—correlate with clinical symptoms like heart failure and exercise intolerance. The stable elevation of mitochondrial membrane potential and resistance to ROS induction suggest maladaptive remodeling of mitochondrial physiology. These findings position mitochondrial resilience as a therapeutic target, with potential strategies including antioxidants, mtDNA repair agents or metabolic modulators. The dissociation between spike protein exposure and mitochondrial dysfunction highlights the need to explore host-directed mechanisms in PASC pathophysiology. This work advances our understanding of long COVID cardiovascular sequelae and provides a foundation for biomarker development and targeted interventions to mitigate long-term morbidity. Full article
(This article belongs to the Special Issue Advances in Immunology and Inflammation During and After Infectious Diseases)
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15 pages, 3061 KiB  
Article
Antiviral Effect of Melatonin on Caco-2 Cell Organoid Culture: Trick or Treat?
by Milda Šeškutė, Dominyka Žukaitė, Goda Laucaitytė, Rūta Inčiūraitė, Mantas Malinauskas and Lina Jankauskaitė
Int. J. Mol. Sci. 2024, 25(22), 11872; https://doi.org/10.3390/ijms252211872 - 5 Nov 2024
Cited by 1 | Viewed by 1493
Abstract
Melatonin is a hormone naturally produced by the body that has recently been found to have antiviral properties. However, its antiviral mechanisms are not entirely understood. Using Caco-2 cells, we developed a gastrointestinal organoid model to investigate the impact of melatonin on cellular [...] Read more.
Melatonin is a hormone naturally produced by the body that has recently been found to have antiviral properties. However, its antiviral mechanisms are not entirely understood. Using Caco-2 cells, we developed a gastrointestinal organoid model to investigate the impact of melatonin on cellular organoid culture response to Poly I:C-induced viral inflammation in the gastrointestinal tract. Melatonin was found to have different effect when applied as a pretreatment before the induction of viral inflammation or as a treatment after it. Melatonin pretreatment after Poly I:C stimulation did not protect organoids from size reduction but enhanced cell proliferation, especially when lower (1 and 10 µM) melatonin concentrations were used. On the other hand, treatment with melatonin after the induction of viral inflammation helped to maintain the size of the organoids while reducing cell proliferation. In pretreated cells, reduced IFNLR1 expression was found, while melatonin treatment increased IFNLR1 expression and reduced the production of viral cytokines, such as IFNλ1 and STAT1-3, but did not prevent from apoptosis. The findings of this study emphasize the importance of type III IFNs in antiviral defense in epithelial gastrointestinal cells and shed more light on the antiviral properties of melatonin as a potential therapeutic substance. Full article
(This article belongs to the Special Issue Advances in Immunology and Inflammation During and After Infectious Diseases)
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17 pages, 1752 KiB  
Review
Endoplasmic Reticulum Stress in Tuberculosis: Molecular Bases and Pathophysiological Implications in the Immunopathogenesis of the Disease
by Jorge Sousa, Lívia Caricio Martins, Julia Moura, Amanda Pereira, Bárbara Vasconcelos, Gustavo Ferro, Pedro Vasconcelos and Juarez Quaresma
Int. J. Mol. Sci. 2025, 26(10), 4522; https://doi.org/10.3390/ijms26104522 - 9 May 2025
Viewed by 255
Abstract
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is a severe pulmonary disease with high mortality, particularly in low-income countries. Early diagnosis and timely treatment, including both intensive and maintenance phases, are critical for controlling the disease and preventing its transmission. In Brazil, where [...] Read more.
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is a severe pulmonary disease with high mortality, particularly in low-income countries. Early diagnosis and timely treatment, including both intensive and maintenance phases, are critical for controlling the disease and preventing its transmission. In Brazil, where TB incidence remains high, thousands of new cases are reported annually. Transmission occurs primarily through airborne droplets expelled by infected individuals. The immune response involves various cell types, such as lymphocytes and macrophages, which form granulomas to limit the spread of the bacillus. Upon entering the lungs, Mtb is phagocytosed by immune cells, where it evades destruction by blocking phagolysosome formation and inhibiting phagosome acidification. In response, the immune system forms granulomas that contain the infection, although these can become reactivated if immune function deteriorates. Mtb also interferes with host cellular organelles, particularly the endoplasmic reticulum (ER) and mitochondria, inducing cellular stress and apoptosis, which aids in its survival. Key Mtb-secreted proteins, such as BAG2 and CdhM, modulate autophagy and apoptosis pathways, influencing pathogen survival within immune cells. A deeper understanding of these molecular mechanisms, particularly the role of ER stress and its impact on immune responses, is essential for developing novel therapeutic strategies for TB prevention and treatment. Full article
(This article belongs to the Special Issue Advances in Immunology and Inflammation During and After Infectious Diseases)
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16 pages, 2428 KiB  
Review
Virus-Induced Pathogenic Antibodies: Lessons from Long COVID and Dengue Hemorrhage Fever
by Der-Shan Sun, Te-Sheng Lien and Hsin-Hou Chang
Int. J. Mol. Sci. 2025, 26(5), 1898; https://doi.org/10.3390/ijms26051898 - 22 Feb 2025
Viewed by 1275
Abstract
Virus-induced antibodies represent a dual-edged sword in the immune response to viral infections. While antibodies are critical for neutralizing pathogens, some can paradoxically exacerbate disease severity through mechanisms such as antibody-dependent enhancement (ADE), autoantibody, and prolonged inflammation. Long coronavirus disease (COVID) and dengue [...] Read more.
Virus-induced antibodies represent a dual-edged sword in the immune response to viral infections. While antibodies are critical for neutralizing pathogens, some can paradoxically exacerbate disease severity through mechanisms such as antibody-dependent enhancement (ADE), autoantibody, and prolonged inflammation. Long coronavirus disease (COVID) and dengue hemorrhagic fever (DHF) exemplify conditions where pathogenic antibodies play a pivotal role in disease progression. Long COVID is associated with persistent immune dysregulation and autoantibody production, leading to chronic symptoms and tissue damage. In DHF, pre-existing antibodies against dengue virus contribute to ADE, amplifying viral replication, immune activation, and vascular permeability. This review explores the mechanisms underlying these pathogenic antibody responses, highlighting the shared pathways of immune dysregulation and comparing the distinct features of both conditions. By examining these studies, we identify key lessons for therapeutic strategies, vaccine design, and future research aimed at mitigating the severe outcomes of viral infections. Full article
(This article belongs to the Special Issue Advances in Immunology and Inflammation During and After Infectious Diseases)
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24 pages, 4314 KiB  
Review
Is the Complement System Dysregulated in Preeclampsia Comorbid with HIV Infection?
by Sumeshree Govender, Mikyle David and Thajasvarie Naicker
Int. J. Mol. Sci. 2024, 25(11), 6232; https://doi.org/10.3390/ijms25116232 - 5 Jun 2024
Cited by 3 | Viewed by 1570
Abstract
South Africa is the epicentre of the global HIV pandemic, with 13.9% of its population infected. Preeclampsia (PE), a hypertensive disorder of pregnancy, is often comorbid with HIV infection, leading to multi-organ dysfunction and convulsions. The exact pathophysiology of preeclampsia is triggered by [...] Read more.
South Africa is the epicentre of the global HIV pandemic, with 13.9% of its population infected. Preeclampsia (PE), a hypertensive disorder of pregnancy, is often comorbid with HIV infection, leading to multi-organ dysfunction and convulsions. The exact pathophysiology of preeclampsia is triggered by an altered maternal immune response or defective development of maternal tolerance to the semi-allogenic foetus via the complement system. The complement system plays a vital role in the innate immune system, generating inflammation, mediating the clearance of microbes and injured tissue materials, and a mediator of adaptive immunity. Moreover, the complement system has a dual effect, of protecting the host against HIV infection and enhancing HIV infectivity. An upregulation of regulatory proteins has been implicated as an adaptive phenomenon in response to elevated complement-mediated cell lysis in HIV infection, further aggravated by preeclamptic complement activation. In light of the high prevalence of HIV infection and preeclampsia in South Africa, this review discusses the association of complement proteins and their role in the synergy of HIV infection and preeclampsia in South Africa. It aims to identify women at elevated risk, leading to early diagnosis and better management with targeted drug therapy, thereby improving the understanding of immunological dysregulation. Full article
(This article belongs to the Special Issue Advances in Immunology and Inflammation During and After Infectious Diseases)
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